Targeting regulated necrotic cell death may reduce kidney inflammation and scarring by disrupting pathways driven by receptor-interacting protein kinases.
This review synthesised current evidence on regulated necrotic cell death in chronic kidney disease, focusing on its molecular definition, key signalling mechanisms, and pharmacological approaches that may inhibit this form of cell death. It examined how receptor-interacting protein kinase pathways connect cellular injury with inflammation and fibrosis across experimental models of kidney disease.
The reviewed evidence indicates that regulated necrotic cell death contributes to chronic kidney disease progression by promoting inflammatory responses, tissue damage, and fibrotic scarring. Increased expression of receptor-interacting protein kinase 3 in experimental kidney disease models supports its pathogenic role and identifies this signalling pathway as a potentially valuable therapeutic target.
